Clostridium difficile was first isolated in 1935 by Hall and O'Toole who proposed the name `difficile' because it was very difficult to isolate. In 1940 Snyder isolated Cl. difficile from infants aged 10 weeks to 1 year. No further isolations were reported until 1960, when the organism was cultured by McBee from the intestinal contents of a seal, and in 1962 Smith and King reported its presence in human infections.1
Cl. difficile is closely related to the Clostridium botulinum, the bacterium responsible for botulism. Cl. difficile is described as spore bearing, gram positive, straight or slightly curved rods with slightly rounded ends. Cl. difficile can be found in soil, stool and intestines of healthy people and animals, uncooked meat or poultry, and spores are easily transferred from the hands of those preparing it.2
The source breakdown is as follows:
• feces of nondiarrheic humans: 5-10%
• hospital environment: up to 25% of patients
• soil, marine sediments (mostly spores)
• dogs and cats: up to 35%
• wide variety of other animals3The anaerobic bacilli can produce a whole host of destructive enzymes such as fibrinolysins, collagenase, lecithinase, and cytolysins. Cl. difficile is in the Risk Group 2 and is not to be exported or imported.4
These enzymes are responsible for the breakdown and destruction of the hoof wall in horses’ feet. In a symbiotic relationship, Cl. difficile with the fungus Geotrichum work together in the confines of the hoof wall. The Geotrichum proceeds to digest the damaged decaying hoof while providing metabolites to the Cl. difficile, and together cause lameness in the animal. 5
Cl. difficile is the major cause of antibiotic-associated diarrhea and pseudomembraneous colitis in humans. Cl. difficile was associated with colitis and diarrhea without pseudomembraneous changes after antibiotic therapy following gastrointestinal operations. After antibiotics deplete the number of other microorganism types, the Cl. difficile has free reign over the environment.
Cl. difficile has two destructive protein toxins, A and B, which cause cellular damage associated with the disease pseudomembraneous colitis. Toxin A of Cl. difficile is an enterotoxin that causes fluid accumulation in the intestines, while Toxin B, a cytopathic agent, damages the cells almost to the point of cell death.
Treatments for infection by this pathogen range from cessation of antibiotics while treating with an anti-C. difficile drug to fecal enema to restore normal intestinal flora. While in the horse hoof infection, treatment with a broad-spectrum topical antimicrobial with the highly effective active ingredient, sodium oxychlorosene.
Prevention is the best defense against Cl. difficile. The practice of good hygiene at home and in the medical community is the number one deterrent. The administering of Saccharomyces boulardii (a non-pathenogenic yeast) and toxin-neutralizing antibodies in elderly patients before gastrointestinal surgery, can deter the Cl. difficile from flourishing.
Sources
1 http://www.oxoid.com/uk/index.asp; Oxoid Product, Clostridium difficile agar base MSDS
2 microvet.arizona.edu/Courses/MIC420/lecture_notes/lecture_cover/lecture_cover.html , Lecture Notes, Pathogenic Bacteriology, by Dr. Glenn Songer
3 http://www.sbsequine.com/report1.html; Taking the Mystery out of White Line Disease – SBS Shoe Bond System, Dr. Richard Shakalis and Dr. John Pautienis
4 http://www.dsmz.de/bactnom/bactname.htm, A service provided by the DSMZ-Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH, Braunschweig, Germany
5 http://www.horseshoes.com/advice/whitelinedisease/dunivant2/dunivant2.htm "White Line Disease, " "Onychomycosis," "Stall Rot," "Hollow Foot," "Wall Thrush," "Yeast Infection," "Seedy Toe" - What is it?
© Richard Dunivant*Disclaimer - This report was written by a student participaring in a microbiology course at the Missouri University of Science and Technology. The accuracy of the contents of this report is not guaranteed and it is recommended that you seek additional sources of information to verify the contents.
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